Acta neuropathologica communications · 2022
Müller cell degeneration and microglial dysfunction in the Alzheimer's retina.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Xu Qinyuan Alis, Boerkoel Pierre, Hirsch-Reinshagen Veronica, Mackenzie Ian R, Hsiung Ging-Yuek Robin, Charm Geoffrey, To Elliott F, Liu Alice Q, Schwab Katerina, Jiang Kailun, Sarunic Marinko, Beg Mirza Faisal, Pham Wellington, Cui Jing, To Eleanor, Lee Sieun, Matsubara Joanne A
Аннотация
Amyloid beta (Aβ) deposits in the retina of the Alzheimer's disease (AD) eye may provide a useful diagnostic biomarker for AD. This study focused on the relationship of Aβ with macroglia and microglia, as these glial cells are hypothesized to play important roles in homeostasis and clearance of Aβ in the AD retina. Significantly higher Aβ load was found in AD compared to controls, and specifically in the mid-peripheral region. AD retina showed significantly less immunoreactivity against glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS) compared to control eyes. Immunoreactivity against ionized calcium binding adapter molecule-1 (IBA-1), a microglial marker, demonstrated a higher level of microgliosis in AD compared to control retina. Within AD retina, more IBA-1 immunoreactivity was present in the mid-peripheral retina, which contained more Aβ than the central AD retina. GFAP co-localized rarely with Aβ, while IBA-1 co-localized with Aβ in more layers of control than AD donor retina. These results suggest that dysfunction of the Müller and microglial cells may be key features of the AD retina.